The onset of and successful progression through puberty carries significant implications for an adolescent’s development with puberty radically altering a child’s physical, psychological, and social baseline. Puberty depends on the proper development of both the Hypothalamic-Pituitary-Gonadal (HPG) Axis and the Adrenal Axis. Hormones from these sources result in observable changes. In 1962, James M. Tanner developed the Sexual Maturity Rating Scale (SMR).[1] This scale, also known as the Tanner stages, granted providers objective criteria to monitor an adolescent’s progression through puberty. By evaluating the development of the testes, breast tissue, and pubic hair, a clinician can counsel and manage their patients through this critical period appropriately. 

It is crucial to understand the limitations of SMR when evaluating patients. SMR only measures the external signs of sexual development obtained via physical exam, and this can limit their use in non-clinical settings. [2] Additionally, the time of onset and rapidity of sexual maturity varies among different ethnicities. There is evidence of advancement in the timing of sexual maturation among a variety of populations; this is observable within both developed and underdeveloped societies, and the underlying cause remains unidentified. However, it is highly likely to be a multifactorial issue that relies on both social and physiological components. It is imperative to have recent and reliable data from a similar population subset to evaluate a patient properly using the SMR.[3][4]

The onset of puberty in both males and females relies on the hypothalamus. The intermittent release of GnRH from the hypothalamus, also known as the hypothalamic pulse generator, signals the release of LH and FSH from the anterior pituitary. There is a postulate that neurotransmitters GABA and Kisspeptin inhibit the release of GnRH. As an individual matures, the hypothalamus becomes less sensitive to this inhibition and eventually shifts towards pulsatile surges.[5][6]

In males, LH stimulates Leydig cells within the testes to produce testosterone, typically occurring between ages 9 to 14. Testosterone can then be converted into its more potent counterpart, dihydrotestosterone (DHT) peripherally via the 5-alpha-reductase enzyme. Testosterone acts on intracellular androgen receptors. It is responsible for the pubertal growth spurt, closure of the epiphyseal plates, deepening of the voice, penile and testicular enlargement, muscle growth, and libido. DHT acts similarly on intracellular receptors yet contributes to facial hair growth, sebaceous gland secretion, and male pattern baldness. 5-alpha-reductase inhibitors have become first-line therapy for the treatment of male pattern baldness.[7][8]

In females, both LH and FSH contribute to the development of secondary sexual characteristics. FSH promotes follicular maturation within the ovary. Theca cells within the follicle are responsive to LH surges releasing testosterone into the periphery. Adjacent granulosa cells, stimulated by FSH, convert testosterone to estrogen via aromatase. Estrogen then goes on to act on intracellular receptors within various tissues resulting in growth spurts, closure of the epiphyseal plates, genital enlargement, and breast tissue development.[9][10]

Puberty is also marked by increased adrenal androgen production, a period called adrenarche. Adrenarche typically occurs around age six. While a specific signaling molecule has to date eluded researchers, it results from increased androgen producing enzymes within the zona reticularis (ZR) layer of the adrenal gland. Dehydroepiandrosterone (DHEA) acts on intracellular receptors promoting androgen-dependent hair growth. Adrenarche is a common pathway between both sexes resulting in shared pubic hair growth patterns.[11]

Breasts

Breast tissue development in the female marks the first secondary characteristic to develop in puberty. Free estrogen acts on intracellular receptors to promote the development of both ductal and stromal elements. The fatty stromal elements compose the majority of breast growth during puberty, and by its completion, there is still only a minor amount of ductal tissue present within the breast. Pregnancy and its associated hormonal changes result in the progression towards increased ductal tissue versus stroma.[12]

Testicles

In males, the growth of the testes beyond 4 mL marks the onset of puberty. Testosterone not bound to either albumin or sex hormone-binding globulin (SHBG) acts on intracellular receptors resulting in increased DNA transcription. It is the rapid expansion of the seminiferous tubules and an increase in germ cell number that contributes to testicular growth patterns.[13][14][7]

Pubic Hair

DHEA and DHEAS both result in the production of pubic and axillary hair growth. These hormones act on follicles, causing both thickening and darkening of the resultant hair. The distribution of hair follicles highly responsive to these hormones is genetically determined. Thus, individuals may be predisposed to a greater distribution of darkened body hair.[15]